How the brain's cerebral cortex functions, and how this function goes awry in diseases like autism and mental retardation, remain unknown. A powerful model system to investigate cortical function is the whisker somatosensory cortex (S1) of rodents. Rodent S1 is a canonical primary sensory area whose cellular and circuit properties are known in remarkable detail, but how these circuits process sensory information is unknown. We propose to investigate how S1 encodes and processes sensory information, which is a critical step to developing an integrated, cellular-to- systems level understanding of cortical function. The resulting description of normal sensory cortical function will help identify the processing defects in autism, mental retardation, and other neurological disorders. To study sensory processing, we focus on sensation of surface texture, which is a basic component of tactile sensation. We will study quantitatively how surface texture is transformed into a pattern of vibrations by the sensory periphery (the whiskers, which function similarly to human fingertips), and encoded by action potentials in populations of neurons in S1. We use the gold-standard technique of quantitatively comparing psychometric, neurometric, and whisker kinetic-based sensory discrimination functions to identify potential sensory codes for texture. In addition, we use modern optogenetics techniques to activate cortical neurons using light, which allows us to perturb neural activity in S1 and determine how different features of cortical spike trains provide sensory information to the animal. Together, these studies will identify the physical and neurobiological signals that convey information about surface texture in somatosensory cortex. This work will contribute to understanding the nature of cortical information processing, and how it is implemented by specific neurons, circuits, and synapses in S1. Conservation of primary sensory cortical function across mammals suggests that principles of sensory processing identified here will be relevant to the human brain. Because rodent S1 is a major disease model for Fragile X mental retardation, epilepsy and other disorders, our work could help establish how these diseases impair cortical function. This work may be particularly relevant for autism, which involves deficits in vibrotactile processing, and whose circuit basis may be revealed by studying defects in S1 processing in rodent models.